Protective effects of β‐casofensin, a bioactive peptide from bovine β‐casein, against indomethacin‐induced intestinal lesions in rats. Issue 4 (3rd February 2016)

• Record Type: Journal Article
• Authors: Bessette, Claudine; Benoit, Bérengère; Sekkal, Soraya; Bruno, Jérémie; Estienne, Monique; Léonil, Joelle; Ferrier, Laurent; Théodorou, Vassilia; Plaisancié, Pascale
• Is Part Of: Molecular nutrition & food research. Volume 60:Issue 4(2016)
• Page Start: 823
• Page End: 833
• Publication Date: 2016-02-03
• Subjects: Milk bioactive peptide -- Mucus -- Intestinal protection -- Functional food -- Inflammatory bowel disease; Food -- Biotechnology -- Periodicals; Food -- Microbiology -- Periodicals; Nutrition -- Periodicals; Food -- Toxicology -- Periodicals; Nutrition -- Periodicals; Food Microbiology -- Periodicals; Food Technology -- Periodicals; Molecular Biology -- Periodicals; 664.0705
• DOI: 10.1002/mnfr.201500680
• Languages: English
• ISSNs: 1613-4125

Abstract

Abstract : The preventive administration of β‐casofensin causes goblet cell hyperplasia and the presence of a copious mucus gel between the villi. This compensates for the decline in mucus production induced by indomethacin injection and reduces intestinal injuries. β‐casofensin also exerts an anti‐apoptotic effect, thereby preserving the epithelial barrier. Finally, if intestinal injuries occur, β‐casofensin accelerates the epithelial restitution. All of these mechanisms of action contribute to decreased severity of enteritis induced by indomethacin. Abstract : Scope: β‐casofensin, also known as peptide β‐CN(94‐123), is a milk bioactive peptide that modulates the intestinal barrier through its action on goblet cells. Here, we evaluated whether oral administration of β‐casofensin can prevent indomethacin‐induced injury of the jejunum in rats. Methods and results: Rats received β‐casofensin (0.01–100 μM) or tap water by daily gavage (4 μL/g) for eight days, then two subcutaneous injections of indomethacin (10 mg/kg, days 9 and 10) and were euthanized on day 12. In vitro, we investigated the effects of β‐casofensin on the restitution of a wounded monolayer. Preventive administration of β‐casofensin (100 μM) reduced intestinal macroscopic and microscopic damage induced by indomethacin. β‐casofensin also prevented the depletion of goblet cells and increased myeloperoxidase activity, as well as tumor necrosis factor‐ɑ (TNF‐ɑ) expression and immunostaining of active caspase‐3 in the jejunum of rats treated with indomethacin. In wound healing experiments, β‐casofensin promoted epithelial restitution with no effect on cell proliferation. This effect was inhibited by pre‐incubation with an anti‐CC chemokine receptor 6 (CCR6) neutralizing antibody. Conclusions: β‐casofensin exerts protective effects in indomethacin‐induced enteritis through preservation of goblet cells and improvement in wound healing. β‐casofensin could therefore become vital in nutritional programs for the prevention of intestinal diseases.